Inhibitors of respiration, or more specifically, of cytochrome oxidase, can break dormancy in some
seeds, including rice [69,70], barley [71], and lettuce [72], as well as in isolated apple embryos [73]. Ap-
ple embryos also respond to anaerobiosis; holding them in nitrogen for 2 weeks or longer permits subse-
quent germination in air [74]. Other reports indicate that high oxygen tension relieves dormancy in sev-
eral grains [71,75–77]. The similar effects of these conditions that restrict versus promote respiration
suggest that different mechanisms control dormancy at different times and dictate that caution be used in
assigning causal effects to various external factors that influence dormancy. (See Roberts and Smith [78]
for a hypothesis to explain these effects.)
VI. PHYSIOLOGICAL BASIS OF DORMANCY
Despite much effort by scientists, the mechanisms that control dormancy in plants remain a mystery. How-
ever, numerous theories have been proposed to account for the phenomenon. All physiological processes
are ultimately controlled by genes, and progress is being made in identifying genes associated with dor-
mancy. Seeds of Arabidopsis thalianarequire dry storage to break dormancy, but mutants have been iso-
lated that produce nondormant seeds [79,80]. The ability of such seeds to germinate has been associated
with single-gene differences in their ability to synthesize ABA or GA (see later). In maize, genes have been
identified that are responsible for preventing premature germination (viviparity) [81,82]. Again, these genes
appear to regulate the synthesis of, or sensitivity to, ABA [83–86]. Skriver and Mundy [87] and Thomas
[88] have reviewed the effects of these and related genes during embryo development. Single-gene control
of dormancy has also been demonstrated in hazel (Corylus avellana) [89] and in peach (Prunus persica)
[90], although no data are yet available on the mechanisms involved. More comprehensive information on
genetic and molecular approaches to dormancy may be found in Lang [18] and King [91].
Although control of dormancy ultimately lies within the genome, such control must be exerted via
physiological mechanisms. The many theories advanced to explain dormancy can be grouped into three
general categories: nutritional/metabolic deficiencies, blocks to membrane permeability, and excesses or
deficiencies of hormones. Briefly stated, these theories propose that the failure of a seed or bud to grow
results from (1) deficiency of a nutrient(s) or of an enzyme(s) able to metabolize such a nutrient, (2) the
inability of nutrients to reach shoot and/or root apices within the dormant organ, or (3) an excess of a
growth inhibitor(s), a deficiency of a growth promoter(s), or an improper balance between the two within
the meristem and/or adjacent tissues. In general, more attention has been devoted to hormone studies than
to the other two areas of research. Seeds are more convenient for studying dormancy than are buds, for
they are small, self-contained, and thus more easily manipulated.
A. Metabolic Aspects of Dormancy
As Bewley and Black [10] emphasized, “Dormancy cannot be equated with overall metabolic in-
activity... .” Respiration rates of hydrated, dormant seeds of lettuce and cocklebur differ little from those
of nondormant seeds prior to germination, and activity of hydrolytic enzymes is unlikely to be crucial, for
little mobilization of reserves occurs prior to radicle emergence [10]. Nevertheless, many studies have
compared the metabolism of dormant versus nondormant seeds and several investigators have proposed
that dormant tissues are deficient in specific enzymes required for metabolism of carbohydrates, fats,
and/or proteins.
- Nutrient Supply
Stokes [92] differentiated between two types of seed dormancy, with embryo dormancy (“true dor-
mancy”) being responsible for the first and lack of nutrients for the second (nonresting embryo). In the
former, interruption of chilling by exposure to high temperature can negate the effect of previous chilling
by inducing secondary dormancy, and the effects of two or more periods of chilling are less than additive.
In the latter, the effects of chilling are additive and irreversible; interruption by high temperature does not
negate the effects of prior exposure to low temperature.
The response of seeds of the second type is easier to explain, superficially, at least. The embryo is
very small and grows at the expense of the surrounding seed tissues (endosperm and/or nucellus). Chill-
ing stimulates the activity of enzymes that hydrolyze stored reserves, which the embryo cannot otherwise
utilize, to compounds that can be used for growth. Thus in seeds of cowparsnip (Heracleum spho-
172 DENNIS